Infectious
Autoimmune / Encephalopathy Panel
Prion Disease
in morning and afternoon , and 1 mg dose in the evening ). Ten days post-discharge his clonazepam was decreased to 1 mg at nighttime by his primary care physician . At a clinic visit two months post-hospital discharge , his myoclonic movements were significantly improved . He was able to ambulate without an assistive device at home although he reported some difficulty with speech . At five months post-discharge , his speech had become clearer , and he did not display myoclonic jerks or movements . We speculate that the cause of his myoclonus was secondary to immune mediated reaction from COVID infection . Improvement in myoclonic jerks after plasmapheresis sessions could have been related to the removal of non-specific antibodies in the serum secondary to the coronavirus infection .
DISCUSSION
Coronavirus disease 2019 ( COVID-19 ) caused by severe acute respiratory syndrome coronavirus 2 ( SARS-CoV-2 ) has greatly affected various aspects of healthcare and inflicted a wide series of challenges in terms of day-to-day medical practice . COVID-19 primarily affects the respiratory system but has a wide range of neurological complications as well . 1-
TABLE 3 : Laboratory Tests Performed Antibodies Tested
Herpes Simplex Virus 1 and 2 PCR , arbovirus , VDRL , Lyme antibody ,
Angiotensin converting enzyme level , Acetylcholine ganglionic receptor antibody , anti-amphiphysin , antiglial nuclear type 1 , antineuronal nuclear ( ANNA-1 ), ANNA-2 , ANNA-3 , CRMP-5-IgG , neuronal ( V-G ) K + channel , P / Q type calcium channel antibody , purkinje cell cytoplasmic type 1 , 2 , TR , antiglial antibody -3 , antiGAD65 , anti-Ma2 / Ta , aquaporin-4 , NMDAR1 , AMAPAR1 , AMPAR2 , GABA-BR , LGI- 1 antibody , CASPR-2 , DPPX
14-3-3 protein
3
The tendency to invade the olfactory nerve roots and olfactory bulb with subsequent manifestation of anosmia is the most common neurological symptom that has been widely reported . 4 Several mechanisms for such neurological symptoms have been hypothesized , including direct viral insult , local acute inflammation , immune mediated inflammation and endothelial dysfunction . 4-6 Cerebral infarctions , cerebral venous thrombosis secondary to coagulopathy , immune mediated optic neuritis , and encephalitis have also been reported previously . 7 The onset of new movement disorders after COVID-19 infection has been rare ; however , few cases of generalized myoclonus , ataxia , opsoclonus , and diaphragmatic myoclonus were reported previously . 8 The pathophysiology of COVID-19 related movement disorders is unclear at this time . An autoimmune mechanism has been proposed from improvement of symptoms after empiric treatment with steroids , immunoglobulins , and plasmapheresis . 9 Movement disorders in general can be daunting for primary care physicians especially in parts of the country where neurological care is not readily available .
COVID-19 associated neurological complications may include encephalopathy , stroke , epilepsy , Guillain-Barre syndrome , optic neuritis , and cerebral venous thrombosis . 3 , 10 , 11 Myoclonus comprises 67 % of the cases of the hyperkinetic disorders in this patient population . 12 , 13 A potential hypothesis for developmental of neurological symptoms is the neuronal death caused by binding of SARS-CoV-2 virus to angiotensin converting enzyme 2 in the brain . 14
Case reports have included descriptions of effective treatment with high dose steroids , intravenous immunoglobulins , plasma exchange , and anti-seizure medications such as levetiracetam , valproic acid , clonazepam , and lorazepam as well as dexmedeto- midine and ketamine . Outcomes have been variable ; however , the patients improved within four to 12 weeks after receiving these therapies . 12 Of note , there are reports of resolution of neurological symptoms without any treatment or intervention . 15
CONCLUSION
Most cases of post-COVID neurological syndromes respond to immunomodulatory therapy as mentioned above . However , it is important to assess for other causes prior to initiation with treatment as was done in the present case . Such movements can be debilitating and may lead to misdiagnosis if not considered in the context of clinical presentation . Further delay without recognizing the underlying etiology like COVID-19 infection appropriately may lead to a delay in treatment , worsening symptoms , and worsened clinical outcome . Our case adds to the pool of knowledge regarding an atypical presentation of patients associated with COVID-19 infection and potential neurological complications .
REFERENCES
1 . Maury A , Lyoubi A , Peiffer-Smadja N , et al . Neurological manifestations associated with SARS-CoV-2 and other coronaviruses : A narrative review for clinicians . Rev Neurol ( Paris ). 2021 Jan- Feb ; 177 ( 1-2 ): 51-64 .
2 . Wu Y , Xu X , Chen Z , et al . Nervous system involvement after infection with COVID-19 and other coronaviruses . Brain Behav Immun . 2020 Jul ; 87:18-22 .
3 . Correia AO , Feitosa PWG , Moreira JLS , et al . Neurological manifestations of COVID-19 and other coronaviruses : A systematic review . Neurol Psychiatry Brain Res . 2020 Sep ; 37:27-32 .
4 . Najafloo R , Majidi J , Asghari A , et al . Mechanism of Anosmia Caused by Symptoms of COVID-19 and Emerging Treatments . ACS Chem Neurosci . 2021 Oct 20 ; 12 ( 20 ): 3795-3805 .
5 . Baig AM , Khaleeq A , Ali U , et al . Evidence of the COVID-19 virus targeting the CNS : tissue distribution , host-virus interaction , and proposed
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